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14 pages, 3052 KiB

Open AccessArticle

Biomarkers Analysis and Clinical Manifestations in Comorbid Creutzfeldt–Jakob Disease: A Retrospective Study in 215 Autopsy Cases

by Nikol Jankovska, Robert Rusina, Jiri Keller, Jaromir Kukal, Magdalena Bruzova, Eva Parobkova, Tomas Olejar and Radoslav Matej

Biomedicines 2022, 10(3), 680; https://doi.org/10.3390/biomedicines10030680 - 16 Mar 2022

Cited by 5 | Viewed by 2502

Abstract

Creutzfeldt–Jakob disease (CJD), the most common human prion disorder, may occur as “pure” neurodegeneration with isolated prion deposits in the brain tissue; however, comorbid cases with different concomitant neurodegenerative diseases have been reported. This retrospective study examined correlations of clinical, neuropathological, molecular-genetic, immunological, [...] Read more.

Creutzfeldt–Jakob disease (CJD), the most common human prion disorder, may occur as “pure” neurodegeneration with isolated prion deposits in the brain tissue; however, comorbid cases with different concomitant neurodegenerative diseases have been reported. This retrospective study examined correlations of clinical, neuropathological, molecular-genetic, immunological, and neuroimaging biomarkers in pure and comorbid CJD. A total of 215 patients have been diagnosed with CJD during the last ten years by the Czech National Center for Prion Disorder Surveillance. Data were collected from all patients with respect to diagnostic criteria for probable CJD, including clinical description, EEG, MRI, and CSF findings. A detailed neuropathological analysis uncovered that only 11.16% were “pure” CJD, while 62.79% had comorbid tauopathy, 20.47% had Alzheimer’s disease, 3.26% had frontotemporal lobar degeneration, and 2.33% had synucleinopathy. The comorbid subgroup analysis revealed that tauopathy was linked to putaminal hyperintensity on MRIs, and AD mainly impacted the age of onset, hippocampal atrophy on MRIs, and beta-amyloid levels in the CSF. The retrospective data analysis found a surprisingly high proportion of comorbid neuropathologies; only 11% of cases were verified as “pure” CJD, i.e., lacking hallmarks of other neurodegenerations. Comorbid neuropathologies can impact disease manifestation and can complicate the clinical diagnosis of CJD. Full article

(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases 2.0)

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10 pages, 2355 KiB

Open AccessArticle

Phenotypic Heterogeneity among GBA p.R202X Carriers in Lewy Body Spectrum Disorders

by Valerio Napolioni, Carolyn A. Fredericks, Yongha Kim, Divya Channappa, Raiyan R. Khan, Lily H. Kim, Faria Zafar, Julien Couthouis, Guido A. Davidzon, Elizabeth C. Mormino, Aaron D. Gitler, Thomas J. Montine, Birgitt Schüle and Michael D. Greicius

Biomedicines 2022, 10(1), 160; https://doi.org/10.3390/biomedicines10010160 - 12 Jan 2022

Viewed by 2619

Abstract

We describe the clinical and neuropathologic features of patients with Lewy body spectrum disorder (LBSD) carrying a nonsense variant, c.604C>T; p.R202X, in the glucocerebrosidase 1 (GBA) gene. While this GBA variant is causative for Gaucher’s disease, the pathogenic role of this [...] Read more.

We describe the clinical and neuropathologic features of patients with Lewy body spectrum disorder (LBSD) carrying a nonsense variant, c.604C>T; p.R202X, in the glucocerebrosidase 1 (GBA) gene. While this GBA variant is causative for Gaucher’s disease, the pathogenic role of this mutation in LBSD is unclear. Detailed neuropathologic evaluation was performed for one index case and a structured literature review of other GBA p.R202X carriers was conducted. Through the systematic literature search, we identified three additional reported subjects carrying the same GBA mutation, including one Parkinson’s disease (PD) patient with early disease onset, one case with neuropathologically-verified LBSD, and one unaffected relative of a Gaucher’s disease patient. Among the affected subjects carrying the GBA p.R202X, all males were diagnosed with Lewy body dementia, while the two females presented as PD. The clinical penetrance of GBA p.R202X in LBSD patients and families argues strongly for a pathogenic role for this variant, although presenting with a striking phenotypic heterogeneity of clinical and pathological features. Full article

(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases 2.0)

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13 pages, 1530 KiB

Open AccessArticle

Low-Dose Niacin Supplementation Improves Motor Function in US Veterans with Parkinson’s Disease: A Single-Center, Randomized, Placebo-Controlled Trial

by Chandramohan Wakade, Raymond Chong, Marissa Seamon, Sharad Purohit, Banabihari Giri and John C. Morgan

Biomedicines 2021, 9(12), 1881; https://doi.org/10.3390/biomedicines9121881 - 10 Dec 2021

Cited by 8 | Viewed by 6655

Abstract

A six-month double-blind, placebo-controlled randomized study was conducted to ascertain whether low-dose daily niacin supplementation would improve motor symptoms in Parkinson’s disease (PD) patients. A total of 47 PD patients were assigned to receive low-dose niacin or a placebo. At the end of [...] Read more.

A six-month double-blind, placebo-controlled randomized study was conducted to ascertain whether low-dose daily niacin supplementation would improve motor symptoms in Parkinson’s disease (PD) patients. A total of 47 PD patients were assigned to receive low-dose niacin or a placebo. At the end of the double-blind phase, all participants received open-label niacin for the next six months. All patients were evaluated at baseline, after six months, and after one year of treatment. The primary outcome measure was the Unified Parkinson’s Disease Rating Scale III (UPDRS III) scores. Secondary outcome measures were depression, sleep quality, mental flexibility and cognition, and physical fatigue. Niacin treatment was well-tolerated by forty-five subjects. The mean [95% CI] change in UPDRS III scores at six months of placebo was −0.05 [95% CI, −2.4 to 2.32], and niacin was −1.06 [95% CI, −3.68 to 1.57]. From six to twelve months when both groups received open-label niacin supplementation, the average UPDRS III scores significantly decreased for the placebo group by 4.58 [95% CI, −0.85 to 8.30] and the niacin group by 4.63 [95% CI, 1.42 to 7.83] points. Low-dose niacin supplementation is a well-tolerated adjunct therapy and may improve motor function in PD when taken over a longer period. Full article

(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases 2.0)

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17 pages, 18005 KiB

Open AccessArticle

Transthyretin as a Biomarker to Predict and Monitor Major Depressive Disorder Identified by Whole-Genome Transcriptomic Analysis in Mouse Models

by Sung-Liang Yu, Selina Shih-Ting Chu, Min-Hui Chien, Po-Hsiu Kuo, Pan-Chyr Yang and Kang-Yi Su

Biomedicines 2021, 9(9), 1124; https://doi.org/10.3390/biomedicines9091124 - 31 Aug 2021

Cited by 6 | Viewed by 2331

Abstract

Background: Accumulations of stressful life events result in the onset of major depressive disorder (MDD). Comprehensive genomic analysis is required to elucidate pathophysiological changes and identify applicable biomarkers. Methods: Transcriptomic analysis was performed on different brain parts of a chronic mild stress (CMS)-induced [...] Read more.

Background: Accumulations of stressful life events result in the onset of major depressive disorder (MDD). Comprehensive genomic analysis is required to elucidate pathophysiological changes and identify applicable biomarkers. Methods: Transcriptomic analysis was performed on different brain parts of a chronic mild stress (CMS)-induced MDD mouse model followed by systemic analysis. QPCR and ELISA were utilized for validation in mice and patients. Results: The highest numbers of genes with significant changes induced by CMS were 505 in the amygdala followed by 272 in the hippocampus (twofold changes; FDR, p < 0.05). Enrichment analysis indicated that the core-enriched genes in CMS-treated mice were positively enriched for IFN-γ response genes in the amygdala, and hedgehog signaling in the hippocampus. Transthyretin (TTR) was severely reduced in CMS-treated mice. In patients with diagnosed MDD, serum concentrations of TTR were reduced by 48.7% compared to controls (p = 0.0102). Paired samples from patients with MDD demonstrated a further 66.3% increase in TTR at remission compared to the acute phase (p = 0.0339). Conclusions: This study provides comprehensive information on molecular networks related to MDD as a basis for further investigation and identifies TTR for MDD monitoring and management. A clinical trial with bigger patient cohort should be conducted to validate this translational study. Full article

(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases 2.0)

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23 pages, 3212 KiB

Open AccessArticle

Antibody Protection against Long-Term Memory Loss Induced by Monomeric C-Reactive Protein in a Mouse Model of Dementia

by Elisa García-Lara, Samuel Aguirre, Núria Clotet, Xenia Sawkulycz, Clara Bartra, Lidia Almenara-Fuentes, Cristina Suñol, Rubén Corpas, Peter Olah, Florin Tripon, Andrei Crauciuc, Mark Slevin and Coral Sanfeliu

Biomedicines 2021, 9(7), 828; https://doi.org/10.3390/biomedicines9070828 - 16 Jul 2021

Cited by 11 | Viewed by 3817

Abstract

Monomeric C-reactive protein (mCRP), the activated isoform of CRP, induces tissue damage in a range of inflammatory pathologies. Its detection in infarcted human brain tissue and its experimentally proven ability to promote dementia with Alzheimer’s disease (AD) traits at 4 weeks after intrahippocampal [...] Read more.

Monomeric C-reactive protein (mCRP), the activated isoform of CRP, induces tissue damage in a range of inflammatory pathologies. Its detection in infarcted human brain tissue and its experimentally proven ability to promote dementia with Alzheimer’s disease (AD) traits at 4 weeks after intrahippocampal injection in mice have suggested that it may contribute to the development of AD after cerebrovascular injury. Here, we showed that a single hippocampal administration of mCRP in mice induced memory loss, lasting at least 6 months, along with neurodegenerative changes detected by increased levels of hyperphosphorylated tau protein and a decrease of the neuroplasticity marker Egr1. Furthermore, co-treatment with the monoclonal antibody 8C10 specific for mCRP showed that long-term memory loss and tau pathology were entirely avoided by early blockade of mCRP. Notably, 8C10 mitigated Egr1 decrease in the mouse hippocampus. 8C10 also protected against mCRP-induced inflammatory pathways in a microglial cell line, as shown by the prevention of increased generation of nitric oxide. Additional in vivo and in vitro neuroprotective testing with the anti-inflammatory agent TPPU, an inhibitor of the soluble epoxide hydrolase enzyme, confirmed the predominant involvement of neuroinflammatory processes in the dementia induced by mCRP. Therefore, locally deposited mCRP in the infarcted brain may be a novel biomarker for AD prognosis, and its antibody blockade opens up therapeutic opportunities for reducing post-stroke AD risk. Full article

(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases 2.0)

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14 pages, 1286 KiB

Open AccessArticle

Foveal Avascular Zone and Choroidal Thickness Are Decreased in Subjects with Hard Drusen and without High Genetic Risk of Developing Alzheimer’s Disease

by Inés López-Cuenca, Rosa de Hoz, Celia Alcántara-Rey, Elena Salobrar-García, Lorena Elvira-Hurtado, José A. Fernández-Albarral, Ana Barabash, Federico Ramírez-Toraño, Jaisalmer de Frutos-Lucas, Juan J. Salazar, Ana I. Ramírez and José M. Ramírez

Biomedicines 2021, 9(6), 638; https://doi.org/10.3390/biomedicines9060638 - 2 Jun 2021

Cited by 8 | Viewed by 3568

Abstract

A family history (FH+) of Alzheimer’s disease (AD) and ɛ4 allele of the ApoE gene are the main genetic risk factors for developing AD, whereas ɛ4 allele plays a protective role in age-related macular degeneration. Ocular vascular changes have been reported in both [...] Read more.

A family history (FH+) of Alzheimer’s disease (AD) and ɛ4 allele of the ApoE gene are the main genetic risk factors for developing AD, whereas ɛ4 allele plays a protective role in age-related macular degeneration. Ocular vascular changes have been reported in both pathologies. We analyzed the choroidal thickness using optical coherence tomography (OCT) and the foveal avascular zone (FAZ) using OCT-angiography and compared the results with ApoE gene expression, AD FH+, and the presence or absence of hard drusen (HD) in 184 cognitively healthy subjects. Choroidal thickness was statistically significantly different in the (FH−, ɛ4−, HD+) group compared with (i) both the (FH−, ɛ4−, HD−) and the (FH+, ɛ4+, HD+) groups in the superior and inferior points at 1500 μm, and (ii) the (FH+, ɛ4−, HD+) group in the superior point at 1500 μm. There were statistically significant differences in the superficial FAZ between the (FH+, ɛ4−, HD+) group and (i) the (FH+, ɛ4−, HD−) group and (ii) the (FH+, ɛ4+, HD−) group. In conclusion, ocular vascular changes are not yet evident in participants with a genetic risk of developing AD. Full article

(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases 2.0)

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20 pages, 3744 KiB

Open AccessEditor’s ChoiceArticle

Alteration in the Cerebrospinal Fluid Lipidome in Parkinson’s Disease: A Post-Mortem Pilot Study

by Joaquín Fernández-Irigoyen, Paz Cartas-Cejudo, Marta Iruarrizaga-Lejarreta and Enrique Santamaría

Biomedicines 2021, 9(5), 491; https://doi.org/10.3390/biomedicines9050491 - 29 Apr 2021

Cited by 30 | Viewed by 5179

Abstract

Lipid metabolism is clearly associated to Parkinson’s disease (PD). Although lipid homeostasis has been widely studied in multiple animal and cellular models, as well as in blood derived from PD individuals, the cerebrospinal fluid (CSF) lipidomic profile in PD remains largely unexplored. In [...] Read more.

Lipid metabolism is clearly associated to Parkinson’s disease (PD). Although lipid homeostasis has been widely studied in multiple animal and cellular models, as well as in blood derived from PD individuals, the cerebrospinal fluid (CSF) lipidomic profile in PD remains largely unexplored. In this study, we characterized the post-mortem CSF lipidomic imbalance between neurologically intact controls (n = 10) and PD subjects (n = 20). The combination of dual extraction with ultra-performance liquid chromatography-electrospray ionization quadrupole-time-of-flight mass spectrometry (UPLC-ESI-qToF-MS/MS) allowed for the monitoring of 257 lipid species across all samples. Complementary multivariate and univariate data analysis identified that glycerolipids (mono-, di-, and triacylglycerides), saturated and mono/polyunsaturated fatty acids, primary fatty amides, glycerophospholipids (phosphatidylcholines, phosphatidylethanolamines), sphingolipids (ceramides, sphingomyelins), N-acylethanolamines and sterol lipids (cholesteryl esters, steroids) were significantly increased in the CSF of PD compared to the control group. Interestingly, CSF lipid dyshomeostasis differed depending on neuropathological staging and disease duration. These results, despite the limitation of being obtained in a small population, suggest extensive CSF lipid remodeling in PD, shedding new light on the deployment of CSF lipidomics as a promising tool to identify potential lipid markers as well as discriminatory lipid species between PD and other atypical parkinsonisms. Full article

(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases 2.0)

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24 pages, 1628 KiB

Open AccessArticle

Determinants of Schizophrenia Endophenotypes Based on Neuroimaging and Biochemical Parameters

by Amira Bryll, Wirginia Krzyściak, Paulina Karcz, Maciej Pilecki, Natalia Śmierciak, Marta Szwajca, Anna Skalniak and Tadeusz J. Popiela

Biomedicines 2021, 9(4), 372; https://doi.org/10.3390/biomedicines9040372 - 1 Apr 2021

Cited by 8 | Viewed by 3528

Abstract

Despite extensive research, there is no convincing evidence of a reliable diagnostic biomarker for schizophrenia beyond clinical observation. Disorders of glutamatergic neurotransmission associated with N-methyl-D-aspartate (NMDA) receptor insufficiency, neuroinflammation, and redox dysregulation are the principal common mechanism linking changes in the periphery with [...] Read more.

Despite extensive research, there is no convincing evidence of a reliable diagnostic biomarker for schizophrenia beyond clinical observation. Disorders of glutamatergic neurotransmission associated with N-methyl-D-aspartate (NMDA) receptor insufficiency, neuroinflammation, and redox dysregulation are the principal common mechanism linking changes in the periphery with the brain, ultimately contributing to the emergence of negative symptoms of schizophrenia that underlie differential diagnosis. The aim of the study was to evaluate the influence of these systems via peripheral and cerebral biochemical indices in relation to the patient’s clinical condition. Using neuroimaging diagnostics, we were able to define endophenotypes of schizophrenia based on objective laboratory data that form the basis of a personalized approach to diagnosis and treatment. The two distinguished endophenotypes differed in terms of the quality of life, specific schizophrenia symptoms, and glutamatergic neurotransmission metabolites in the anterior cingulate gyrus. Our results, as well as further studies of the excitatory or inhibitory balance of microcircuits, relating the redox systems on the periphery with the distant regions of the brain might allow for predicting potential biomarkers of neuropsychiatric diseases, including schizophrenia. To the best of our knowledge, our study is the first to identify an objective molecular biomarker of schizophrenia outcome. Full article

(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases 2.0)

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Review

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15 pages, 1184 KiB

Open AccessReview

Serum-Based Biomarkers in Neurodegeneration and Multiple Sclerosis

by Patrizia LoPresti

Biomedicines 2022, 10(5), 1077; https://doi.org/10.3390/biomedicines10051077 - 6 May 2022

Cited by 10 | Viewed by 7238

Abstract

Multiple Sclerosis (MS) is a debilitating disease with typical onset between 20 and 40 years of age, so the disability associated with this disease, unfortunately, occurs in the prime of life. At a very early stage of MS, the relapsing-remitting mobility impairment occurs [...] Read more.

Multiple Sclerosis (MS) is a debilitating disease with typical onset between 20 and 40 years of age, so the disability associated with this disease, unfortunately, occurs in the prime of life. At a very early stage of MS, the relapsing-remitting mobility impairment occurs in parallel with a progressive decline in cognition, which is subclinical. This stage of the disease is considered the beginning of progressive MS. Understanding where a patient is along such a subclinical phase could be critical for therapeutic efficacy and enrollment in clinical trials to test drugs targeted at neurodegeneration. Since the disease course is uneven among patients, biomarkers are needed to provide insights into pathogenesis, diagnosis, and prognosis of events that affect neurons during this subclinical phase that shapes neurodegeneration and disability. Thus, subclinical cognitive decline must be better understood. One approach to this problem is to follow known biomarkers of neurodegeneration over time. These biomarkers include Neurofilament, Tau and phosphotau protein, amyloid-peptide-β, Brl2 and Brl2-23, N-Acetylaspartate, and 14-3-3 family proteins. A composite set of these serum-based biomarkers of neurodegeneration might provide a distinct signature in early vs. late subclinical cognitive decline, thus offering additional diagnostic criteria for progressive neurodegeneration and response to treatment. Studies on serum-based biomarkers are described together with selective studies on CSF-based biomarkers and MRI-based biomarkers. Full article

(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases 2.0)

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12 pages, 980 KiB

Open AccessReview

Movement Disorders in Oncology: From Clinical Features to Biomarkers

by Luca Marsili, Alberto Vogrig and Carlo Colosimo

Biomedicines 2022, 10(1), 26; https://doi.org/10.3390/biomedicines10010026 - 23 Dec 2021

Cited by 5 | Viewed by 3369

Abstract

Background: the study of movement disorders associated with oncological diseases and anticancer treatments highlights the wide range of differential diagnoses that need to be considered. In this context, the role of immune-mediated conditions is increasingly recognized and relevant, as they represent treatable disorders. [...] Read more.

Background: the study of movement disorders associated with oncological diseases and anticancer treatments highlights the wide range of differential diagnoses that need to be considered. In this context, the role of immune-mediated conditions is increasingly recognized and relevant, as they represent treatable disorders. Methods: we reappraise the phenomenology, pathophysiology, diagnostic testing, and treatment of movement disorders observed in the context of brain tumors, paraneoplastic conditions, and cancer immunotherapy, such as immune-checkpoint inhibitors (ICIs). Results: movement disorders secondary to brain tumors are rare and may manifest with both hyper-/hypokinetic conditions. Paraneoplastic movement disorders are caused by antineuronal antibodies targeting intracellular or neuronal surface antigens, with variable prognosis and response to treatment. ICIs promote antitumor response by the inhibition of the immune checkpoints. They are effective treatments for several malignancies, but they may cause movement disorders through an unchecked immune response. Conclusions: movement disorders due to focal neoplastic brain lesions are rare but should not be missed. Paraneoplastic movement disorders are even rarer, and their clinical-laboratory findings require focused expertise. In addition to their desired effects in cancer treatment, ICIs can induce specific neurological adverse events, sometimes manifesting with movement disorders, which often require a case-by-case, multidisciplinary, approach. Full article

(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases 2.0)

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18 pages, 397 KiB

Open AccessReview

An Overview of ICA/BSS-Based Application to Alzheimer’s Brain Signal Processing

by Wenlu Yang, Alexander Pilozzi and Xudong Huang

Biomedicines 2021, 9(4), 386; https://doi.org/10.3390/biomedicines9040386 - 6 Apr 2021

Cited by 11 | Viewed by 3211

Abstract

Alzheimer’s disease (AD) is by far the most common cause of dementia associated with aging. Early and accurate diagnosis of AD and ability to track progression of the disease is increasingly important as potential disease-modifying therapies move through clinical trials. With the advent [...] Read more.

Alzheimer’s disease (AD) is by far the most common cause of dementia associated with aging. Early and accurate diagnosis of AD and ability to track progression of the disease is increasingly important as potential disease-modifying therapies move through clinical trials. With the advent of biomedical techniques, such as computerized tomography (CT), electroencephalography (EEG), magnetoencephalography (MEG), positron emission tomography (PET), magnetic resonance imaging (MRI), and functional magnetic resonance imaging (fMRI), large amounts of data from Alzheimer’s patients have been acquired and processed from which AD-related information or “signals” can be assessed for AD diagnosis. It remains unknown how best to mine complex information from these brain signals to aid in early diagnosis of AD. An increasingly popular technique for processing brain signals is independent component analysis or blind source separation (ICA/BSS) that separates blindly observed signals into original signals that are as independent as possible. This overview focuses on ICA/BSS-based applications to AD brain signal processing. Full article

(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases 2.0)

13 pages, 582 KiB

Open AccessReview

Mechanistic Insights into Alzheimer’s Disease Unveiled through the Investigation of Disturbances in Central Metabolites and Metabolic Pathways

by Raúl González-Domínguez, Álvaro González-Domínguez, Ana Sayago, Juan Diego González-Sanz, Alfonso María Lechuga-Sancho and Ángeles Fernández-Recamales

Biomedicines 2021, 9(3), 298; https://doi.org/10.3390/biomedicines9030298 - 14 Mar 2021

Cited by 11 | Viewed by 3059

Abstract

Hydrophilic metabolites are closely involved in multiple primary metabolic pathways and, consequently, play an essential role in the onset and progression of multifactorial human disorders, such as Alzheimer’s disease. This review article provides a comprehensive revision of the literature published on the use [...] Read more.

Hydrophilic metabolites are closely involved in multiple primary metabolic pathways and, consequently, play an essential role in the onset and progression of multifactorial human disorders, such as Alzheimer’s disease. This review article provides a comprehensive revision of the literature published on the use of mass spectrometry-based metabolomics platforms for approaching the central metabolome in Alzheimer’s disease research, including direct mass spectrometry, gas chromatography-mass spectrometry, hydrophilic interaction liquid chromatography-mass spectrometry, and capillary electrophoresis-mass spectrometry. Overall, mounting evidence points to profound disturbances that affect a multitude of central metabolic pathways, such as the energy-related metabolism, the urea cycle, the homeostasis of amino acids, fatty acids and nucleotides, neurotransmission, and others. Full article

(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases 2.0)

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